ArticleAlzheimer's research & therapy2013
Comprehensive behavioral characterization of an APP/PS-1 double knock-in mouse model of Alzheimer's disease.
Article in Alzheimer's research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 146 citations in OpenAlex.
- Exploring the Neuroprotective Effects of Walnut (International journal of molecular sciences · 2026Article
- The default mode network exhibits circuit-specific selective vulnerability despite widespread amyloid burden in an animal model of Alzheimer's disease.Nature communications · 2026Article
- Fructose Intake Is Associated with Brain Metabolic Reprogramming and Exacerbation of Alzheimer-like Alterations in APP/PS1 Mice.International journal of molecular sciences · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- 40-Hz transauricular vagal nerve stimulation rescues cognition of 9-month-old APP/PS1 mice via inhibiting hippocampal P2X7 receptor signaling.Frontiers in aging neuroscience · 2026Article
- Circadian rhythm of amyloid-β in the olfactory bulb and cerebellum of wild-type and APPxPS1 knock-in mice indicates a loss of rhythmicity in regions more vulnerable to amyloid pathology.Biogerontology · 2025Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Interferon signaling modulates Down syndrome-associated Alzheimer's disease pathology in a mouse model.iScience · 2025Article
- Interactions between daily sleep-wake rhythms, γ-secretase, and amyloid-β peptide pathology point to complex underlying relationships.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Impaired hippocampal circuit function underlying memory encoding and consolidation precede robust Aβ deposition in a mouse model of alzheimer's disease.Scientific reports · 2025Article
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Gene-dose-dependent reduction of Fshr expression improves spatial memory deficits in Alzheimer's mice.Molecular psychiatry · 2025Article
- Impaired hippocampal circuit function underlying memory encoding and consolidation precede robust Aβ deposition in a mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- The role ofFrontiers in neuroscience · 2025Review
- Exploring the Impact of Semaglutide on Cognitive Function and Anxiety-Related Behaviors in a Murine Model of Alzheimer's Disease.Biomedicines · 2024Article
- Amino Acid Compound 2 (AAC2) Treatment Counteracts Insulin-Induced Synaptic Gene Expression and Seizure-Related Mortality in a Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Intestinal endogenous metabolites affect neuroinflammation in 5×FAD mice by mediating "gut-brain" axis and the intervention with Chinese Medicine.Alzheimer's research & therapy · 2024Article
- Loss of GDE2 leads to complex behavioral changes including memory impairment.Behavioral and brain functions : BBF · 2024Article
- Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases.Current issues in molecular biology · 2024Review
29 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
Funding
Abstract
introductionDespite the extensive mechanistic and pathological characterization of the amyloid precursor protein (APP)/presenilin-1 (PS-1) knock-in mouse model of Alzheimer's disease (AD), very little is known about the AD-relevant behavioral deficits in this model. Characterization of the baseline behavioral performance in a variety of functional tasks and identification of the temporal onset of behavioral impairments are important to provide a foundation for future preclinical testing of AD therapeutics. Here we perform a comprehensive behavioral characterization of this model, discuss how the observed behavior correlates with the mechanistic and pathological observations of others, and compare this model with other commonly used AD mouse models.
methodsFOUR DIFFERENT GROUPS OF MICE RANGING ACROSS THE LIFESPAN OF THIS MODEL (TEST GROUPS: 7, 11, 15, and 24 months old) were run in a behavioral test battery consisting of tasks to assess motor function (grip strength, rotor rod, beam walk, open field ambulatory movement), anxiety-related behavior (open field time spent in peripheral zone vs. center zone, elevated plus maze), and cognitive function (novel object recognition, radial arm water maze).
resultsThere were no differences in motor function or anxiety-related behavior between APP/PS-1 knock-in mice and wild-type counterpart mice for any age group. Cognitive deficits in both recognition memory (novel object recognition) and spatial reference memory (radial arm water maze) became apparent for the knock-in animals as the disease progressed.
conclusionThis is the first reported comprehensive behavioral analysis of the APP/PS1 knock-in mouse model of AD. The lack of motor/coordination deficits or abnormal anxiety levels, coupled with the age/disease-related cognitive decline and high physiological relevance of this model, make it well suited for utilization in preclinical testing of AD-relevant therapeutics.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.